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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >TSU-68 Ameliorates Hepatocellular Carcinoma Growth by Inhibiting Microenvironmental Platelet-derived Growth Factor Signaling
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TSU-68 Ameliorates Hepatocellular Carcinoma Growth by Inhibiting Microenvironmental Platelet-derived Growth Factor Signaling

机译：TSU-68通过抑制微环境血小板衍生的生长因子信号转导来改善肝癌的生长

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摘要

Background: TSU-68 is a multikinase inhibitor that targets platelet-derived growth factor receptors (PDGFRs). In the present study, we evaluated the effect of TSU-68 on the tumor-microenvironment interaction in hepatocellular carcinoma (HCC). Materials and Methods: HCC and fibroblast cell lines (HuH7, Hep3B, HuH1 and WI-38) were used to evaluate their interactions. Cancer characteristics were evaluated by spheroid formation and tumorigenicity in immunodeficient mice. Time-lapse image analysis was performed to monitor cell motility. Results: Although PDGFA was abundantly expressed, PDGFR-alpha was predominantly located in the cytoplasm and was not functional in HuH7 cells. Co-culture experiments demonstrated that HCC cells induced phosphorylation of PDGFR-alpha in WI-38 fibroblasts and that stimulated fibroblasts, in turn, boosted the spheroid formation capacity of HCC cells. TSU-68 inhibited phosphorylation of PDGFR-alpha in WI-38 cells and suppressed the growth of subcutaneously co-injected HuH7/WI-38 tumor xenografts. Conclusion: TSU-68 inhibits stromal PDGF signaling activated by cancer cells and suppresses HCC growth.
机译：背景：TSU-68是一种多激酶抑制剂，靶向血小板衍生的生长因子受体（PDGFR）。在本研究中，我们评估了TSU-68对肝细胞癌（HCC）肿瘤-微环境相互作用的影响。材料和方法：HCC和成纤维细胞系（HuH7，Hep3B，HuH1和WI-38）用于评估它们之间的相互作用。通过免疫缺陷小鼠中的球状体形成和致瘤性评估癌症特征。进行延时图像分析以监测细胞运动。结果：尽管PDGFA大量表达，但PDGFR-α主要位于细胞质中，在HuH7细胞中不起作用。共培养实验表明，HCC细胞在WI-38成纤维细胞中诱导了PDGFR-α的磷酸化，而刺激成纤维细胞反过来又增强了HCC细胞的球状形成能力。 TSU-68抑制WI-38细胞中PDGFR-α的磷酸化，并抑制皮下共注射的HuH7 / WI-38肿瘤异种移植物的生长。结论：TSU-68抑制癌细胞激活的基质PDGF信号传导并抑制HCC生长。

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